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Published on: January 9, 2019
Apoptosis in Gliomas: Molecular Mechanisms and Therapeutic Implications
Joachim P Steinbach1, Michael Weller
1Hertie Institute for Clinical Brain Research, Department of General Neurology, School of Medicine, University of Tübingen, Tübingen, Germany, michael.weller@uni-tuebingen.de.
Abstract:
Understanding apoptosis is often considered a key to understand the genesis of tumors and to devise innovative strategies for their treatment. Similar to other types of cancer, essential pathways regulating apoptosis are also disrupted in malignant gliomas, notably the cell cycle control mechanisms regulated by the p53 and retinoblastoma (RB) proteins and their homologs. Moreover, cultured glioma cells appear not to activate the extrinsic death receptor-dependent apoptotic pathway in response to irradiation or cytotoxic drugs. A preferential expression of antiapoptotic rather than proapoptotic BCL-2 family proteins and high level expression of inhibitor-of-apoptosis proteins (IAP) may be responsible for the failure of glioma cells to activate caspases in response to apoptotic stimuli. Although apoptosis does occur spontaneously in malignant gliomas in vivo, there is little evidence that the current modes of non-surgical treatment, radiotherapy and chemotherapy, mediate their effects via induction of apoptosis, with the possible exception of anaplastic oligodendrogliomas which often show striking tumor regression on neuroimaging. Yet, the induction of apoptosis plays a conceptual role in the majority of novel experimental approaches to malignant glioma which are currently evaluated in cell culture and preclinical rodent models.
Insights
Understanding apoptosis is crucial for cancer genesis and treatment. Malignant gliomas disrupt apoptosis pathways, often resisting cell death induction by standard therapies, necessitating novel treatment strategies.
Area of Science:
- Oncology
- Molecular Biology
- Cell Death Research
Background:
- Apoptosis (programmed cell death) is vital for tumor development and cancer therapy.
- Malignant gliomas, aggressive brain tumors, exhibit dysregulated apoptosis pathways.
- Key regulators like p53 and retinoblastoma (RB) proteins are implicated in glioma cell cycle control and apoptosis resistance.
Purpose of the Study:
- To investigate the role and regulation of apoptosis in malignant gliomas.
- To understand why glioma cells resist apoptosis induction by common cancer treatments.
- To identify potential therapeutic targets for enhancing apoptosis in gliomas.
Main Methods:
- Analysis of apoptosis regulatory pathways in glioma cells.
- Assessment of glioma cell response to cytotoxic drugs and irradiation.
- Evaluation of antiapoptotic and proapoptotic protein expression (BCL-2 family, IAP).
Main Results:
- Glioma cells show impaired activation of the extrinsic apoptotic pathway.
- Overexpression of antiapoptotic proteins (BCL-2 family, IAP) contributes to caspase inhibition.
- While spontaneous apoptosis occurs in vivo, conventional therapies show limited induction of apoptosis in most gliomas.
Conclusions:
- Malignant gliomas possess intrinsic resistance to apoptosis induction.
- Targeting apoptosis pathways is a key strategy for novel glioma therapies.
- Further research into overcoming apoptosis resistance is essential for effective brain tumor treatment.
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